ArticleJournal of molecular neuroscience : MN2014
Krüppel-like factor 8 ameliorates Alzheimer's disease by activating β-catenin.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- Krüppel-like factors family in health and disease.MedComm · 2024Review
- Bioinformatic Evaluation ofGenes · 2024Article
- A Single-Cell Transcriptomic Analysis of the Mouse Hippocampus After Voluntary Exercise.Molecular neurobiology · 2024Article
- New Insights into lncRNAs in Aβ Cascade Hypothesis of Alzheimer's Disease.Biomolecules · 2022Review
- Young transposable elements rewired gene regulatory networks in human and chimpanzee hippocampal intermediate progenitors.Development (Cambridge, England) · 2022Article
- Interaction of NF-κB and Wnt/β-catenin Signaling Pathways in Alzheimer's Disease and Potential Active Drug Treatments.Neurochemical research · 2021Review
- Aberrant Excitatory-Inhibitory Synaptic Mechanisms in Entorhinal Cortex Microcircuits During the Pathogenesis of Alzheimer's Disease.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Regulation of Krüppel-like factor 8 by the NEDD4 E3 ubiquitin ligase.American journal of translational research · 2019Article
- ERK2 phosphorylates Krüppel-like factor 8 protein at serine 48 to maintain its stability.American journal of cancer research · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A sustained loss of Wnt signaling function may be involved in the pathology of Alzheimer's disease (AD). Krüppel-like factor 8 (KLF8) induces the activation of Wnt/β-catenin signaling pathway. Thus, KLF8 may be related with the risk of AD. We want to know the role of KLF8 in the development of AD. A rat brain slice model for AD was established. Quantitative RT-PCR, western blotting, and fluorescence staining assays were carried out to examine the effects of KLF8 on the protein expression of some important molecules, which are associated with the development of AD. The enhanced expression level of KLF8 could increase the protein expression level of β-catenin, which interacted with and inhibited nuclear factor-kappa B (NF-κB). The protein levels of KLF8 and β-catenin were increased, while the level of NF-κB was decreased in the AD model. The inhibition of NF-κB was followed by the decrease of the protein expression levels of amyloid precursor protein (APP) and phosphorylated tau (Phospho-Tau). The protein level of KLF8 was decreasing from stages I to IV in patients with AD. This study provides evidence that KLF8 can inhibit the progression of AD.
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